Lecture 27: Pathology of ovary and uterus Flashcards
(42 cards)
How does HPV link to cancer formation?
Carinomas
epithelial origin - adenocarcinoma: adrenal epithelium - squamous cell carcinoma: squamous epithelium simple epi --> carcinoma glandular --> adenocarcinoma squamous --> squamous cell carcinoma urothelium --> urothelial carcinoma
Lymphoma
lymphoid tissue origin
- Hodgkin’s disease
- Non- Hodgkins ( T or B cells)
Melanoma
melanocytic cell adipose tissue --> liposarcoma neural tissue --> malignant peripheral nerve sheath bone --> osteosarcoma Cartilage --> chondosarcoma muscle --> leiomyo/Rhabdomyosarcoma
Sarcoma
mesenchymal (structural cells , holding fat, nerves and bones )
- less common
Where can uterine pathologies occur
Uterus + Neighbouring structures: rectum, bladder, sigmoid colon
Note: Ovarian pathologies can easily spread
Follicle quantities in the ovary
400,000 primordial follicles –> dormant until puberty –> FSH and Lh release causes 20 follicles to mature each cycle –> 1 out of the twenty reaches maturity and is released –> Menopause –> only a few follicles remain
Ovary in H&M section (hameotocilin and EOSM slide)
cortex, stroma, mesothelial lining, follicles, BV, hilum
3x Main ovarian tumours
Metastases spread from everywhere to the ovary–>
- Germ: germ cell tumours (teratoma)
- Stromal: sex cord stromal tumours (fibroma)
- Surface: majority of ovarian tumours arise from the surface/fimbrial end of the Fallopian tube
What sort of structure is the ovary inherently?
Cystic structure
- ovaries are constantly forming follicular cysts which develop –> mature –> rupture
Ovarian tumour table
Polycystic ovaries
In cortex –> follicles proliferate but never ovulated –> continued oestrogen stimulation –> no ovulation (no progesterone) –> endometrial hyperplasia and carcinoma
Polycystic ovaries: follicular cyst (never popped)
Ovarian neoplasm
multi cystic (solid) areas
- -> once malignant they become increasingly solid
1. cyst adenoma
2. mucinous cyst adenomas
3. serous
4. mucinous carcinoma
5. serous carcinoma
Histological features of ovarian neoplasm
- large nuclei
2. course chromatin
Dermoid cyst/Teratomas
dermoid cyst –> females try to make baby WITHOUT MALE SPERM –> starts forming structures (e.g. teeth, hair) –> but recapitulates and goes completely wrong
- normally benign, sitting in skin for years
pot. to develop squamous cel carcinoma in skin
relationship b/w stomach and ovary
diffuse gastric cell carcinoma –> often metastasises into ovary
- another stomach carcinoma is Putinburg Signet Ring carcinoma
relationship b/w colon and ovary
colorectal carcinoma –> can metastasise –> become cystic –> mimic primary ovarian neoplasm
Putinburg carcinoma
Signet ring cell carcinoma (of stomach) –> nucleus on top and cytoplasm below –>
length of normal fallopian tube
9-11 cm
What does the fallopian tube open into
peritoneal cavity
Function of Fallopian tube
ovulation –> follicle rupture and fimbrae align overtop –> ovum enters lumen of FT –> FERTILIZATION occurs in fallopian tubes –> BlastoCYTE move through rest of fallopian tube into Uterus –> blastocyte IMPLANTS into uterus after several days
Structure of Fallopian Tube
Plicae: fingerlike projections Lining: serous columnar epithelium cilia: brush egg down towards uterus - smooth muscle wall lining Overall: delicate and complex structure that is very vulnerable to inflammation and tumours --> stops plicae movement --> unable to direct egg --> complications
Fallopian Tube tumour table
Bilateral Salphangitis
Enflamed fimbrial ends stick together –> fallopian tubes fill with puss and blood